In normal energy production ATP is formed by oxidative phosphorylation. For processes requiring energy, a high energy phosphate group is split from the ATP molecule releasing energy, and the ATP becomes ADP. Under normal conditions this ADP is rapidly oxidatively rephosphorylated to ATP. However if in sufficient oxygen is present the formation of ATP is slowed or abolished. Under these conditions the ADP is further broken down to AMP or IMP. If hypoxia persists the degradation of the adenine nucleotides will proceed and the ultimate compound formed is uric acid. All of the steps in the degradation process, with the exception of the final two steps which result in the formation of uric acid, are either directly or indirectly reversible. However, once uric acid is formed, it represents an amount of energy base which has been irreversibly lost from the cells. Previous studies from this laboratory have quantitated the loss of adenine nucleotides from the myocardial cells during hypoxia produced by cardiac arrest and have related their decline to survival. The present study investigates the possibility of protecting the adenine energy bases from irreversible degradation during cardiac arrest. The approach to this problem involves the use of various enzyme blocking agents to alter the degradation process and prevent the formation of uric acid during cardiac arrest and recovery. The primary agent under consideration is allopurinol. The theory of the project is that if the breakdown products of the energy bases can be retained in the cells in a form from which resynthesis of ATP is possible when sufficient oxygen becomes present then survival should be improved. A corollary study will investigate the possibility of correcting the loss of the adenine nucleotides after it has already occurred during cardiac arrest. Treatment will consist of the use of enzyme blockers as well as exogenous replenishment of some of the intermediate compounds required for the resynthesis of ATP. An additional phase of study will deal with the role of the adenine nucleotides in occlusive coronary disease and in instances of myocardial infarction.